Abstract
Dilated cardiomyopathy (DCM) is associated with a high incidence of arrhythmias leading to sudden death, but little is known about the underlying basis for these arrhythmias. To understand the mechanistic basis for lethal arrhythmias in idiopathic DCM, the properties of the myocardium in terms of its arrhythmogenicity, were studied using a mouse model of inherited DCM with a deletion mutation in the cardiac troponin T gene (TNNT2) which decreases Ca2+ sensitivity of myofilaments. Ventricular myocardium and single myocytes were obtained from wild-type (WT) and DCM mice.
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